Vibrio, Campylobacter, Helicobacter PDF

Vibrio, Campylobacter, Helicobacter BY: Dr. Halimi DEPARTMENT OF MICROBIOLOGY SCHOOL OF MEDICINE TEHRAN UNIVERSITY OF MEDICAL SCIENCE  Gram negative bacteria...

Vibrio, Campylobacter, Helicobacter BY: Dr. Halimi DEPARTMENT OF MICROBIOLOGY SCHOOL OF MEDICINE TEHRAN UNIVERSITY OF MEDICAL SCIENCE  Gram negative bacteria Facultative Anaerobic Aerobic Anaerobic Microaerophilic Bacteroides fragilis Pseudomonas Enterobacteriaceae Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 2  Enterobacteriaceae E.coli Salmonella Shigella Typhoidal Salmonellae Yersinia EHEC S. flexneri Y. pestis Nontyphoidal S. boydii Y. enterocolitica ETEC Salmonellae S. sonnei Y. pseudotuberculosis EPEC S. dysenteriae EAEC UPEC Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 3  Gram negative bacteria Facultative Anaerobic Aerobic Anaerobic Microaerophilic Bacteroides fragilis Pseudomonas Vibrio Enterobacteriaceae Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 4  Vibrionaceae
Gram-negative Facultatively anaerobic Straight, curved, or comma-shaped rods Motile Halophile


Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 5 Vibrio Isolated from a wide variety of
intestinal and extraintestinal human illnesses. The genus is composed of 119 species of curved rods. Three species are particularly important human pathogens :  Vibrio cholerae  Vibrio parahaemolyticus  Vibrio vulnificus 6 Vibrio, Campylobacter, Helicobacter(Dr.Halimi)  Epidemiology of V. cholerae  Cholera is associated: With poor sanitation Direct contact with contaminated surface water
Asymptomatically infected humans can also be an important reservoir for this organism in areas where V. cholerae disease is endemic Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 7 Physiology and Structure V. cholera can grow: On a variety of simple media without additional salt Within a broad temperature range (from 14° C to 40° C) V. cholera is susceptible to stomach acids. Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 8  Physiology and Structure There are more than 200 serogroups of V. cholera.  V. cholerae O1 serotypes  Inaba Ogawa Hikojima biotypes Classical El Tor  V. cholerae O139 Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 9 V. cholerae life cycle Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 10  Pathogenesis of Vibrio cholera 1 2 Passage through the stomach via Polar flagella 3 Colonize the small intestine via Toxin co-regulated pilus 4 Causes the secretory diarrhea via Cholera toxin  Complex A-B toxin 5  Functionally similar to the heat-labile enterotoxin of Escherichia  Promote chloride ion (Cl−) secretion coli  Decreased absorption by villous cells  Increase Cyclic adenosine monophosphate (cAMP)  Water moves from epithelial cells into the bowel lumen Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 11 Clinical Diseases  The clinical manifestations of cholera begin An average of 2 to 3 days after ingestion of the bacteria With the abrupt onset of watery diarrhea and vomiting  As more fluid is lost The feces-streaked stool specimens become  Colorless  Odorless  Free of protein, and speckled with mucus (“rice-water” stools) Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 12 Pathogenesis of Vibrio cholera low-grade fever muscle pains nausea vomiting abdominal cramps Metabolic acidosis (bicarbonate loss) severe diarrhea (“rice-water” stools) Hypokalemia Hypovolemic shock (potassium loss) Loss of renal function Respiratory and cardiac failure Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 13 Laboratory Diagnosis Specimen collection  Early in the disease and inoculated promptly onto culture media. If culture will be delayed, the specimen should be mixed in a Cary-Blair transport medium and refrigerated. Vibrios have low survival rates in buffered glycerol-saline Direct Detection of V. cholerae O1 in Stool Dark-field or phase contrast microscopy Molecular Detection in Clinical Specimens

Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 14 Laboratory Diagnosis Culture Vibrios grow on most media used in clinical laboratories for stool and wound cultures, including: Enrichment broth (e.g., alkaline peptone broth, pH 8.6) Blood agar Mac- Conkey agar Thiosulfate citrate bile salts sucrose [TCBS] agar A chromogenic agar, CHROMagar
Identification Conventional Phenotypic Tests

Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 15  Treatment, Prevention, and Control 1. Fluid and electrolyte replacement How to Approach Rehydration in Patients with Suspected Cholera 2. A single dose of azithromycin Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 16 Treatment, Prevention, and Control  A killed vaccine consisting of:  whole cells of V. cholerae O1 plus recombinant cholera toxin B subunit  Bivalent killed vaccine of whole cells of V. cholera O1 and O139 Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 17 Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 18  V. parahaemolyticus
Source of Infection: Rehydration is usually the only treatment needed Shellfish, seawater Clinical Disease: Gastroenteritis Wound infection Symptoms of include: nausea, vomiting, abdominal cramps, low-grade fever, and chills Bacteremia Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 19  V. vulnificus
Source of Infection: Shellfish, seawater Clinical Disease: Wound infection Septicemia Wound infections may progress to: Cellulitis with extensive necrosis (often requiring surgical debridement) Myositis Necrotizing fasciitis that may mimic gas gangrene Secondary septicemia Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 20  Gram negative bacteria Facultative Facultative Anaerobic Aerobic Microaerophilic Microaerophilic Anaerobic Anaerobic Bacteroides fragilis Pseudomonas Vibrio Enterobacteriaceae Campylobacter Helicobacter Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 21 Campylobacter Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 22 Campylobacter  The genus Campylobacter consists of small, motile, comma-shaped, gram negative rods.  Campylobacteriosis is a worldwide zoonosis  Campylobacter infections are usually sporadic; the incidence starts to rise in March  Outbreaks usually occur in the spring and fall.  Secondary transmission of Campylobacter from ill persons to other individuals is rare





Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 23 Campylobacter  C. jejuni, like Salmonella Typhimurium, is susceptible to hydrochloric acid.  Patients who use proton pump inhibitors or H2 blockers are more susceptible to infection. Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 24  Clinical Diseases  GI infections C. jejuni, C. coli, and C. upsaliensis  Acute enteritis  Diarrhea, fever, and severe abdominal pain  Acute colitis  Abdominal pain mimicking acute appendicitis  Extraintestinal infections: Bacteremia Hepatitis Urinary tract infection Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 25  Clinical Diseases  Guillain-Barré syndrome  C. jejuni and C. upsaliensis An autoimmune disorder of the peripheral nervous system  Reactive arthritis  C. jejuni  Reiter syndrome  C. jejuni Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 26 Common Campylobacter Species Associated with Human Disease A surface (S)-layer protein that functions as a capsule Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 27  Fecal specimens Transport media Laboratory Diagnosis Alkaline peptone water with thioglycolate Stuart medium Cary-Blair medium Collection sample Direct Examination Microscopy Antigen Detection A commercial immunoassay for detection of C. jejuni and C. coli is available Nucleic Acid–Based Tests Culture Skirrow’s,, and Campy-BAP media Campylobacter species require a microaerobic atmosphere
Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 28 Treatment, Prevention, and Control  Campylobacter gastroenteritis is typically a self-limited infection managed by  The replacement of lost fluids and electrolytes Antibiotics Erythromycin or azithromycin Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 29 Gastric helicobacters Enterohepatic helicobacters Helicobacter Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 30  There is no evidence of animal-to-human transmission Helicobacter pylori The O side chain of H. pylori is antigenically similar to the Lewis blood group antigens. H. pylori has occasionally been isolated from Feces, especially from children Dental plaque Saliva Oral-oral transmission Small, curved, microaerophilic, gram-negative rods Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 31 Clinical Consequences Associated with H. pylori Colonization Gastritis Peptic ulcers B-cell lymphomas Gastric adenocarcinoma Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 32 Association of H. pylori colonization and disease states Urease ,Mucinase, Phospholipase Vacuolating cytotoxin A (VacA) Tissue damage Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 33 Laboratory Diagnosis Antigen Detection Antibody Detection 34 Laboratory Diagnosis Invasive tests Rapid urease test Warthin-Starry Giemsa stains Culture Nucleic Acid–Based Tests 35 Treatment, Prevention, and Control Regimens for Initial Treatment  Proton pump inhibitor (e.g., omeprazole)  Macrolide (e.g., clarithromycin)  β-lactam (e.g., amoxicillin) Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 36  Gram negative bacteria Facultative Facultative Anaerobic Aerobic Microaerophilic Microaerophilic Anaerobic Anaerobic Bacteroides fragilis Pseudomonas vibrio Enterobacteriaceae Campylobacter Helicobacter Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 37  Gastrointestinal infection Nosocomial Diarrhea Community Diarrhea/ vomiting Acute watery Persistent Acute C. difficle Dysentery Diarrhea Diarrhea vomiting S. aureus EPEC, ETCE, B. Shigella, C. jejuni, EPEC/ EAEC Bacillus cereus cereus, C. EIEC, perfringens Y. enterocolitica and nontyphoidal salmonella Vibrio, Campylobacter, Helicobacter(Dr.Halimi) 38